It is postulated that by suppressing JAK2 phosphorylation, NOT inhibits JAK2/STAT3 signaling, enhances intracellular ROS burst, and destabilizes VIM, Snail, β-catenin, or N-cadherin oncogene interaction with the stemness marker SOX2 or OCT4, thus suppressing tumorsphere formation and oncogenicity and consequently leading to HCC cell death as expressed by upregulated cleaved PARP levels. Here, JAK2 is linked to hepatocellular carcinoma.